Transcript:

[0:00]

Hi everyone, welcome back to Mad Barn Academy — and if this is your first time tuning in, then welcome! We hope to earn your subscription today. Today's topic for our presentation is going to be on equine proliferative enteropathy, or infection with Lawsonia intracellularis. This is a really important disease of weanling horses, and since late summer and fall are common times of year for a lot of people to be weaning their foals, I thought it would be a great time to discuss EPE. So let's get started.

[0:33]

EPE, or equine proliferative enteropathy, is caused by a bacterial infection. The causative agent is called Lawsonia intracellularis. Lawsonia is an obligate intracellular bacterium — meaning it can only survive and replicate inside a host cell. The cells it invades are the enterocytes, or the cells that line the small intestine.

[1:01]

Infection with Lawsonia intracellularis results in thickening of the intestinal lining, which then results in poor absorption of nutrients out of the gut. It is a disease of young horses, pretty much exclusively, and most frequently seen in foals aged anywhere from four to seven months. Generally, isolated cases are seen on a farm — maybe one foal in a herd is affected — but some farms may experience outbreaks if there are a large number of susceptible foals.

[1:42]

Lawsonia intracellularis is transmitted through the fecal-oral route, meaning the foal consumes feed or forage contaminated with feces containing the bacterium. What we are not 100% sure about is exactly who is doing the contaminating. We think older horses or potentially other foals in a herd may act as asymptomatic carriers, shedding it in their manure. It's also possible that contact with other domestic or wild animals that are carriers can contaminate the environment.

[2:23]

Lawsonia is a well-documented issue in piglets, so adult pigs may act as carriers. It’s also suspected that rodents or other wildlife may serve as reservoirs, but this is still an active area of research. In any case, a carrier species contaminates feed or forage, a susceptible foal ingests the bacteria, and for 5 to 17 days that foal will be contagious — shedding bacteria in manure but not showing clinical signs. This further contaminates the environment and puts other susceptible foals at risk.

[3:14]

Lawsonia intracellularis targets the small intestine, particularly the ileum — the last section that connects to the cecum. Because the bacterium survives inside cells, it’s very good at evading the immune system, which is why foals can have a hard time clearing the infection on their own.

[3:43]

Once an enterocyte is infected, it begins to replicate prematurely and excessively, causing proliferative thickening of the intestinal lining. These cells can’t absorb nutrients normally, resulting in malabsorption. Inflammation in the small intestine also causes protein from the bloodstream to leak into the gut — a condition called protein-losing enteropathy.

[4:22]

The ultrasound image shown here is from a filly with confirmed Lawsonia intracellularis infection. The small intestinal loops have severely thickened walls — measuring 9 mm, compared to the normal ≤3 mm.

[4:53]

Risk factors are not well defined, but stress is thought to be major. Stress compromises the immune system, making disease more likely. Most foals contract Lawsonia between four and seven months — which coincides with weaning, a major stressor. Around the same time, there’s also something called an “immunity gap”: maternal antibodies from colostrum start to wane at about 12 weeks, but the foal’s own immune system isn’t fully mature yet. This creates a window of poor immunity.

[6:00]

This double whammy — decreased immune protection and weaning stress — makes foals particularly susceptible. Other possible risk factors include overcrowding, mixing species, dietary changes, transportation, and recent antibiotic use, which can disrupt the gut microbiome.

[7:15]

Only about 10% of exposed foals become sick, and even fewer develop clinical disease. About half will have subclinical disease, showing signs like suboptimal weight gain or growth. Common clinical signs of EPE include weight loss, poor hair coat, pot belly, loose manure or chronic diarrhea, colic, poor appetite, fever, ventral edema (swelling along the chest, abdomen, and sheath/udder), and occasionally dark or bloody manure. Severe, life-threatening infection is rare but may involve sepsis, collapse, or sudden death.

[8:44]

Diagnosis is based on a combination of physical exam (age, clinical signs), supportive bloodwork (low protein, elevated white blood cells), and ultrasound (intestinal wall thickening). The only definitive test is fecal PCR, which detects bacterial DNA in manure. False negatives can occur, especially early in the disease.

[9:55]

Treatment involves a course of antibiotics, sometimes for several weeks, and supportive care depending on severity. Supportive nutrition is important, as these foals have been malnourished. Highly digestible fiber sources (beet pulp, forage pellets), added fat and protein, and well-balanced, bioavailable vitamins and minerals help recovery.

[11:09]

Prevention focuses on early identification, good biosecurity, and possibly pest and wildlife control. There is also an option to vaccinate — using an off-label swine vaccine — which has shown promising results in reducing incidence and severity. This should be discussed with your veterinarian if EPE is a concern on your farm.

[12:12]

Here are today’s references. Thanks so much for listening! Don’t forget to like and subscribe, and check out our other videos on a variety of topics. I’ve also provided links in the description with more information on EPE, other infectious GI diseases in foals, and colic. Until next time!